1982Journal of Periodontal ResearchRequires access

The effect of indomethacin on alveolar bone loss in experimental periodontitis

Marilyn Weaks‐Dybvig, F Sanavi, Helmut Zander, Barry R. Rifkin

Open publisher page 82 citations

Abstract

This study was undertaken to determine if prostaglandins play a role in the events leading to loss of bone in the ligature model of periodontitis. Periodontitis was induced by placement of the ligatures around mandibular teeth on one side of the jaw of squirrel monkeys (Saimiri sciureus). From one day prior to ligature placement, half the animals were administered indomethacin (5 mg/kg/day), a potent inhibitor of prostaglandin synthesis. Animals were sacrificed after one and two weeks of experimental periodontitis. It was found that indomethacin treatment abolished the significant losses of alveolar bone height and bone mass seen in non‐indomethacin‐treated (NIT) animals following ligature placement. Indomethacin also depressed the large increase in osteoclast density measured at one week in the NIT animals. The results support the hypothesis that prostaglandins are an important mediator of bone loss in the ligature model of periodontitis. Evidence is also presented for the coupling of bone resorption with osteoblastic neo‐osteogenesis on both periodontal ligament and endosteal bone surfaces.

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What this paper is about

This study was undertaken to determine if prostaglandins play a role in the events leading to loss of bone in the ligature model of periodontitis. Periodontitis was induced by placement of the ligatures around mandibular teeth on one side of the jaw of squirrel monkeys (Saimiri sciureus). From one day prior to ligature placement, half the animals were administered indomethacin (5 mg/kg/day), a potent inhibitor of prostaglandin synthesis. Animals were sacrificed after one and two weeks of experimental periodontitis. It was found that indomethacin treatment abolished the significant losses of alveolar bone height and bone mass seen in non‐indomethacin‐treated (NIT) animals following ligature placement. Indomethacin also depressed the large increase in osteoclast density measured at one week in the NIT animals. The results support the hypothesis that prostaglandins are an important mediator of bone loss in the ligature model of periodontitis. Evidence is also presented for the coupling of bone resorption with osteoblastic neo‐osteogenesis on both periodontal ligament and endosteal bone surfaces.

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Available abstract

This study was undertaken to determine if prostaglandins play a role in the events leading to loss of bone in the ligature model of periodontitis. Periodontitis was induced by placement of the ligatures around mandibular teeth on one side of the jaw of squirrel monkeys (Saimiri sciureus). From one day prior to ligature placement, half the animals were administered indomethacin (5 mg/kg/day), a potent inhibitor of prostaglandin synthesis. Animals were sacrificed after one and two weeks of experimental periodontitis. It was found that indomethacin treatment abolished the significant losses of alveolar bone height and bone mass seen in non‐indomethacin‐treated (NIT) animals following ligature placement. Indomethacin also depressed the large increase in osteoclast density measured at one week in the NIT animals. The results support the hypothesis that prostaglandins are an important mediator of bone loss in the ligature model of periodontitis. Evidence is also presented for the coupling of bone resorption with osteoblastic neo‐osteogenesis on both periodontal ligament and endosteal bone surfaces.

Key concepts: Ligature, Dental alveolus, Periodontitis, Periodontal fiber, Bone resorption, Osteoclast, Medicine, Dentistry

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